Laminin mediates the restitution of rat gastric mucosa in vitro

Restitution, the rapid re‐establishment of mucosal integrity following damage, involves cell migration and can be monitored by measuring transmucosal potential difference of tissue mounted in an Ussing chamber. The involvement of extracellular matrix proteins and matrix receptors was examined in the restitution of rat gastric mucosa. Undamaged mucosa maintained a potential difference of ‐32.7 +/− 2.2 mV for several hours. Mucosal exposure to 0.6 M NaCl for 1 min reduced this to −3.3 +/− 1.4 mV in 2‐3 min. Thereafter, the potential difference returned in 60 min to plateau at ‐28.9 +/− 1.3 mV (88.5 +/− 3.6% of pre‐exposure). Tissues mucosally treated with 1:100 anti‐laminin antiserum maximally recovered following damage to 65.6 +/− 6.6% of pre‐exposure potential difference (PD), while those treated with 1:100 anti‐collagen IV or anti‐fibronectin antisera recovered to 88.8 +/− 9.7% and 86.3 +/− 3.2%, respectively. Only the anti‐laminin result was significantly different from controls. The anti‐laminin effect was abolished by pre‐incubation of the anti‐laminin antiserum with purified rat laminin, suggesting that the effect was laminin specific. In experiments involving matrix protein receptors, tissues treated with alpha‐lactalbumin, a protein altering the substrate specificity of cell surface laminin receptor/enzyme beta‐1,4‐galactosyltransferase, maximally recovered following damage to only 49.3 +/− 7.7% of pre‐exposure PD, which was significantly different from controls, while those treated with anti‐beta 1 integrin recovered to 85.0 +/− 9.7%. Our data suggest that laminin is involved in mediation of gastric mucosal restitution, possibly via beta‐1,4‐galactosyltransferase.